2019 journal article
Effect of silver nanoparticles on gill membranes of common carp: Modification of fatty acid profile, lipid peroxidation and membrane fluidity
ENVIRONMENTAL POLLUTION, 256.
author keywords: Toxicity; Silver nanoparticles; Fatty acid; Membrane; Gill
MeSH headings : Animals; Carps / physiology; Fatty Acids / metabolism; Gills / drug effects; Gills / metabolism; Lipid Peroxidation / drug effects; Membrane Fluidity / drug effects; Metal Nanoparticles / toxicity; Silver / toxicity
TL;DR:
The results suggest that the mechanism of AgNPs membrane toxicity involves the oxidization of long-chain omega-3 unsaturated FAs to saturated FAs via lipid peroxidation, resulting in, decreased membrane fluidity and ultimately the destruction of the normal physiological function of the fish gill membrane.
(via Semantic Scholar)
open access via doi.org (publisher)
UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
14. Life Below Water
(OpenAlex)
Source: Web Of Science
Added: January 13, 2020
Although the toxicity of silver nanoparticles (AgNPs) in aquatic organisms has been extensively investigated, the mechanism by which AgNPs damage membranes remains unclear. This study investigated the toxic effects of a series of sub-lethal concentrations of AgNPs on the membranes of freshwater carp (Cyprinus carpio) gills, based on changes in membrane fatty acid (FA) profile, membrane fluidity, membrane lipid peroxidation, and histopathology. Most of the FAs in fish gill membrane was not significantly affected by exposure to multiple AgNPs concentrations, only few significant changes occurred in some specific FAs species at a high concentration of AgNPs exposure. In particular, high concentrations of AgNPs significantly decreased the proportions of two important long-chain n-3 series polyunsaturated FAs (C20: 5n3, and C22: 6n3), resulting in a decreased ratio of n-3 polyunsaturated FAs to n-6 polyunsaturated FAs (Σn-3UFA/Σn-6UFA). The AgNPs also caused a dose-dependent decrease in fish gill membrane fluidity, increased the level of lipid peroxidation, and inhibited Na+/K+-ATPase enzyme activity. Further histopathological examination revealed that exposure to AgNPs can cause toxic responses in the lamellae, including the thinning of the basement membrane, malformation, and inflammation. Together, the results suggest that the mechanism of AgNPs membrane toxicity involves the oxidization of long-chain omega-3 unsaturated FAs to saturated FAs via lipid peroxidation, resulting in, decreased membrane fluidity and ultimately the destruction of the normal physiological function of the fish gill membrane. The findings contribute significantly to our understanding of nanoparticle-induced membrane toxicity and potential risks in aquatic environments.